Endurance training limits the functional alterations of rat heart mitochondria submitted to in vitro anoxia-reoxygenation

• Published in: International journal of cardiology Vol. 109; no. 2; pp. 169 - 178
• Main Authors: Ascensão, António, Magalhães, José, Soares, José M C, Ferreira, Rita, Neuparth, Maria J, Marques, Franklim, Oliveira, Paulo J, Duarte, José A
• Format: Journal Article
• Language: English
• Published: Netherlands 10.05.2006
• Subjects: Animals; Biomarkers - metabolism; Cell Respiration; Chaperonin 60 - metabolism; Citrate (si)-Synthase - metabolism; Disease Models, Animal; Exercise Test; HSP70 Heat-Shock Proteins - metabolism; Hypoxia - metabolism; Hypoxia - physiopathology; Lipid Peroxidation; Male; Mitochondria, Heart - metabolism; Oxidative Phosphorylation; Oxygen Consumption; Physical Conditioning, Animal; Physical Endurance; Protein Carbonylation; Rats; Rats, Wistar
• ISSN: 0167-5273

Studies analysing the effect of endurance training on heart mitochondrial function submitted to in vitro anoxia-reoxygenation (A-R) are missing. The present study aimed to investigate the effect of moderate endurance treadmill training (14 weeks) against rat heart mitochondrial dysfunction induced by in vitro A-R. Respiratory parameters (state 3, state 4, ADP/O and respiratory control ratio-RCR) and oxidative damage markers (carbonyl groups and malondialdehyde) were determined in isolated mitochondria before and after 1 min anoxia followed by 4 min reoxygenation. Levels of heat shock protein 60 kDa (HSP60) and 70 kDa (HSP70) were measured before A-R in mitochondria and whole muscle homogenate, respectively. A-R significantly impaired the rate of state 3 and state 4 respiration, as well as the RCR and ADP/O in the sedentary group. However, mitochondrial state 3 respiration was significantly higher in trained than in the sedentary group both before and after A-R. The impairments in RCR, ADP/O ratio and state 4 induced by A-R in sedentary group were significantly attenuated in endurance-trained group. The inhibition of state 4 induced by GDP was significantly higher in trained than in sedentary group. Oxidative modifications of mitochondrial proteins and phospholipids were found in sedentary group after A-R, although limited in trained group. Increased levels of mitochondrial HSP60 and tissue HSP70 accompanied the lower decrease in the respiratory function after A-R observed in trained group. We therefore concluded that endurance training limited the impairments on rat heart mitochondria caused by the oxidant insult inflicted by in vitro A-R.